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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is emerging evidence that prostate inflammation may contribute to prostatic carcinogenesis. Chronic inflammation has been associated with the development of malignancy in several other organs such as esophagus, stomach, colon, liver and urinary bladder. Inflammation is thought to incite carcinogenesis by causing cell and genome damage, promoting cellular turnover, and creating a tissue microenvironment that can enhance cell replication, angiogenesis and tissue repair. Epidemiological data have correlated prostatitis and sexually transmitted diseases with an increased risk of prostate cancer and intake of anti-inflammatory drugs and antioxidants with a decreased risk. Evidence from genetic and molecular studies also support the hypothesis that prostate inflammation and/or infection may be a cause of prostate cancer. In 1999 De Marzo et al proposed that proliferative inflammatory atrophy (PIA) is a precursor to PIN and cancer. Further research will provide opportunities for the discovery and development of strategies for treatment and prevention of prostate cancer.
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PMID:Inflammation and prostate cancer. 1652 82

One of the most important problems in urological practice is how to differentiate clinically significant and non significant prostate cancer (Pca) i.e. how to avoid over treatment of tumors with low malignant potential in one hand, and inappropriate less aggressive treatment of significant tumors, on the other hand. At the first place, one should estimate precise local clinical stage and the grade of the disease. Transrectal ultrasound--guided prostate biopsy id the golden standard, but there are few dilemmas concerning prostate biopsy: the number of biopsy cores, inter and intra-observer variations in the grading, the significance of PIN, multifocal character of Pca etc. Our opinion is that sextant or octan biopsy is quite sufficient for the exact detection of clinically insignificant cancers. An additional problem is the discrepancy in grade between biopsy and radical prosatectomy specimen. Second, the treatment should not be the same for every patient and it is guided by the age and general condition of the patient. The aggressive treatment is recommendable for younger patients, younger than 70-72 years, even for tiny area of cancer in one of the biopsy samples. On the other hand, it is an ethical question, should we insist on detection of small cancer foci at older patients, and make them anxious and unhappy in their last years of life.
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PMID:Clinically significant and non significant prostate cancer an ongoing question. 1667 90

Incidence of prostate cancer has risen dramatically in the past decade. Radical prostatectomy is indicated in patients who have disease localized to the prostate. The aim of the study is to make histopathological evaluation of radical prostatectomy in the treatment local prostate cancer. Authors analyzed 49 cases of radical prostatectomy due to cancer localized to the prostate in period 1996-2000 in Clinic of Urology in Clinical Center of Serbia, Belgrade. The average age of the patients was 65, 6 years (range 44-76, pick 61-70). The most cases 25 (51%, p < 0.001) we found in pT2a N0M0, in pT2b N1M0 9 (18.36%), in pT3bN0M0 10 (20.4%), in pT3bN1M0 3 (6.12%), in pT4aN0M0 2 (4.08%). Nodal status positive was in 12 cases: 9 (18%) in pT2bN1M0- iliac 3 (right 2, left 1), obturatory 6 (right 1, left 5) and 3 cases in pT3bN1M0-iliac left 1 and obturatory 2 (1 right and 1 left). We found Gleason score 8 in 9 cases (18.36%) in pT2bN1M0 versus 7 cases (14.5%) without nodal metastases. Gleason score 9 we found in 3 cases (6.1%) in pT3bN1M0 versus one case without nodal metastases (difference is not significant). Gleason score 3 was in 6.1%, 4 in 12.2%, 5 in 8.1%, 6 in 16, 3%, 7 in 24.5%. Grade 1 of tumors we found in 9 cases (18%), grade 2 in 11 (22%), grade 3 in 29 (60%). HG PIN was in 18 cases (36.7%), LG PIN in 10 (20.4%). In all cases was elevated PSA: 4-10 mmol/L in 24 pts, 11-20 in 15 pts and > 20 in 10 pts. Radical prostatectomy is most adequate method in surgical treatment cancer localized in the prostate. Pelvic lymphadenectomy is necessary for staging purposes in adenocarcinoma of the prostate. Early detection adenocarcinoma of the prostate is important factor in decreasing rate of death.
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PMID:Histopathological evaluation of radical prostatectomy in the treatment of localized prostate cancer. 1667 6

Human telomerase detected by in situ hybridization has been demonstrated to be a useful tool for the diagnosis of malignancy and has also been tested by reverse transcriptase-polymerase chain reaction in several tumors such as hepatic cell carcinoma, melanoma, colonic carcinoma, gastric carcinoma, biliary carcinoma, breast carcinoma, mesothelioma, lung carcinoma, female tract carcinoma, and prostatic carcinoma. A monoclonal antibody (clone Tel-24) that allows for the detection of human telomerase reverse transcriptase (hTERT) in paraffin blocks of archival material has recently been developed. Carcinomas of cervix, endometrium, and breast have been studied by this method, but its value in prostatic carcinoma has not been explored; for that reason, we studied benign and malignant prostatic lesions by immunohistochemistry using paraffin embedded tissue. The aim of the study was to define the sensitivity and specificity of hTERT in prostate cancer, in comparison with alpha-methylacyl-coenzyme A racemase (AMACR) (P504-S). Fifty-five specimens of diverse prostatic lesions were selected for study (43 needle biopsies and 12 transurethral resections); there were 61 malignancies (47 infiltrating carcinomas and 14 high-grade prostatic intraepithelial neoplasias [PIN]) and 29 benign lesions (10 basal cell hyperplasias, 12 nodular hyperplasias, 4 chronic prostatitis, and 3 atrophic glands). Signal for hTERT nucleolar was detected in 31 of 47 infiltrating adenocarcinomas, in 11 of 14 PIN, and in none of 27 benign lesions (sensitivity, 71%; specificity, 100%). Diffuse cytoplasmic positivity for AMACR was found in 37 of 41 infiltrating adenocarcinomas, in 7 of 7 PIN, and in 6 of 22 benign lesions (sensitivity, 91%; specificity, 72%). These results indicate that hTERT is highly specific of malignancy, with no false-positive cases; however, it had lower sensitivity than AMACR.
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PMID:Human telomerase and alpha-methylacyl-coenzyme A racemase in prostatic carcinoma. A comparative immunohistochemical study. 1684 61

Understanding prostate stem cells (PSCs) may provide insight for the design of therapeutics for prostate cancer. We have developed a quantitative in vivo colony-forming assay and have demonstrated that the Sca-1 antigen is present on the surface of a prostate cell subpopulation that possesses multiple stem cell properties. Immunofluorescent analysis demonstrates that Sca-1 is expressed by both basal and luminal cells in the proximal region of the adult prostate, but is not expressed by either lineage in more distal regions. The proximal region has been suggested as the PSC niche based on BrdU label-retention studies and the presence of distinct smooth-muscle cells that produce high levels of TGF-beta. Sca-1 is also expressed by nearly all cells within fetal prostate epithelial chords, suggesting Sca-1 may be conserved on PSCs throughout development. Malignant epithelial cells from TRAMP mice, as well as normal prostate cells with lentiviral-mediated alteration of the PTEN/AKT signaling pathway, give rise to PIN lesions and prostate cancer in vivo. Alteration of PTEN/AKT signaling in Sca-1-enriched PSCs also results in PIN lesions, suggesting that PSCs can serve as one target for prostate carcinogenesis.
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PMID:Prostate stem cells and prostate cancer. 1686 53

2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine (PhIP) has been implicated as a major mutagenic heterocyclic amine in the human diet and is carcinogenic in the rat prostate. To validate PhIP-induced rat prostatic neoplasia as a model of human prostate cancer progression, we sought to study the earliest histologic and morphologic changes in the prostate and to follow progressive changes over time. We fed sixty-seven 5-week-old male Fischer F344 rats with PhIP (400 ppm) or control diets for 20 weeks, and then sacrificed animals for histomorphologic examination at the ages of 25, 45, and 65 weeks. Animals treated with PhIP showed significantly more inflammation (P = .002, > .001, and .016 for 25, 45, and 65 weeks, respectively) and atrophy (P = .003, > .001, and .006 for 25, 45, and 65 weeks, respectively) in their prostate glands relative to controls. Prostatic intraepithelial neoplasia (PIN) occurred only in PhIP-treated rats. PIN lesions arose in areas of glandular atrophy, most often in the ventral prostate. Atypical cells in areas of atrophy show loss of glutathione S-transferase pi immunostaining preceding the development of PIN. None of the animals in this study developed invasive carcinomas, differing from those in previous reports. Overall, these findings suggest that the pathogenesis of prostatic neoplasia in the PhIP-treated rat prostate proceeds from inflammation to postinflammatory proliferative atrophy to PIN.
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PMID:Inflammation and atrophy precede prostatic neoplasia in a PhIP-induced rat model. 1698 28

Prostatic intraepithelial neoplasia (PIN) is the most established precursor of prostatic carcinoma. The presence of prominent nucleoli within an existing duct structure is an easy way to identify the disorder. Four main patterns of high-grade PIN (HGPIN) have been described: tufting, micropapillary, cribriform, and flat. In addition to exhibiting similar cytologic features, both HGPIN and prostatic carcinoma are associated with increased incidence and severity with age, and with high rates of occurrence in the peripheral zone of the prostate. HGPIN and prostate cancer share genetic and molecular markers as well, with PIN representing an intermediate stage between benign epithelium and invasive malignant carcinoma. The clinical significance of HGPIN is that it identifies patients at risk for malignancy. With the increased use of extended biopsy protocols, clinicians are more likely to identify HGPIN and less likely to miss concurrent carcinoma. Androgen deprivation therapy decreases the prevalence and extent of PIN, and may play a role in chemoprevention. Preliminary studies suggest that selective estrogen receptor modulators may also prevent the progression of HGPIN to prostate cancer.
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PMID:Prostatic intraepithelial neoplasia: an overview. 1698 75

The Rac-specific guanine nucleotide exchange factor, Tiam1, plays a major role in oncogenicity, tumour invasion and metastasis but its usefulness as a prognostic marker in human cancer has not been tested yet. In the present study, Tiam1 expression was analysed in benign secretory epithelium, pre-neoplastic high-grade prostatic intraepithelium neoplasia (HG-PIN) and prostate carcinomas of 60 R0-resected radical prostatectomy specimens by semiquantitative immunohistochemistry. Tiam1 proved significantly overexpressed in both HG-PIN (P<0.001) and prostate carcinomas (P<0.001) when compared to benign secretory epithelium. Strong Tiam1 overexpression (i.e. > or =3.5-fold) in prostate carcinomas relative to the respective benign prostatic epithelium was statistically significantly associated with disease recurrence (P=0.016), the presence of lymph vessel invasion (P=0.031) and high Gleason scores (GS) (i.e. > or =7) (P=0.044). Univariate analysis showed a statistically significant association of strong Tiam1 overexpression with decreased disease-free survival (DFS) (P=0.03). This prognostic effect of strong Tiam1 overexpression remained significant in multivariate analysis including preoperative prostate-specific antigen levels, pT stage, and GS (relative risk= 3.75, 95% confidence interval=1.06-13.16; P=0.04). Together, our data suggest that strong Tiam1 overexpression relative to the corresponding benign epithelial cells is a new and independent predictor of decreased DFS for patients with prostate cancer.
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PMID:Prognostic relevance of Tiam1 protein expression in prostate carcinomas. 1700 80

The aim of the current study was to analyze HER-2 expression and gene amplification in prostate cancer and HGPIN incidentally detected in cystoprostatectomies. Eighty prostate cases were used. Group 1 (incidental): nineteen cystoprostatectomy specimens with prostate cancer and HGPIN and no residual urothelial carcinoma in the prostate. Group 2 (untreated): twenty-five radical prostatectomy specimens with prostate cancer Group 3 (hormonally treated): nineteen radical prostatectomy specimens with prostate cancer. All the patients were under total androgen ablation therapy for three months before surgery. Group 4 (hormone-independent): nine TURP specimens with locally recurrent androgen independent prostate cancer Group 5 (normal reference): eight cystoprostatectomy specimens without HGPIN and without prostate cancer, and no residual urothelial carcinoma. None of the patients belonging to Groups 1, 2, and 5 had received chemotherapy, hormone therapy, or radiation therapy before surgery. Weak to moderate HER-2 membrane immunoreactivity was observed in most of the basal cells but not in the secretory cells of normal prostatic ducts and acini both in the cystoprostatectomies and in the radicals of the untreated patients. High-grade PIN. HER-2 overexpression was present in the secretory cells in 26% of HGPIN cases in the CyP group, 40% in the untreated clinically detected cancer group, and 83% in the treated group. Prostate cancer HER-2 overexpression was seen in 16% of cases in the CyP group, 36% in the untreated group and 47.5% in the treated group. HER-2 overexpression was present in 78% of cases with androgen independent PCa. Association of HER-2 overexpression and gene amplification. When considering HGPIN the lowest proportion of cases with HER-2 overexpression and with nuclei with gene amplification was seen in the CyP specimens (7%), whereas the highest was in the treated material (28%). As far as the cancers were concerned, the proportions were slightly higher than in HGPIN, the lowest value being in the CyP specimens (9%) and the highest in the hormone independent PCa (62.5%). A statistically significant difference in the number of cases with both overexpression and amplification was only seen between CyP and hormone-independent cancers (p = 0.007).
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PMID:HER-2 expression and gene amplification in high-grade PIN and prostate cancer. 1726 16

The methylation status of four genes significant in prostate carcinogenesis p16, HIC1, N33 and GSTP1, were evaluated using quantitative methylationsensitive polymerase chain reaction. Tumor epithelia, tumor-associated stroma, normal epithelia, foci of PIN and benign prostate hyperplasia, and stroma adjacent to tumor tissues were isolated from whole-mount prostatectomy specimens of patients with localized prostate cancer by using laser capture microdissection. We found high levels of gene methylation in the tumor epithelium and tumor-associated stromal cells and some methylation in both hyperplastic epithelium and stromal cells in normal-appearing tissues located adjacent to tumors. Promoter methylation in the non-neoplastic cells of the prostate tumor microenvironment may play an important role in cancer development and progression. We examined the promoter methylation status of pl6, HIC1, N33 and GSTP1 in prostate biopsy fragments and prostate tissues after radical prostatectomy from patients with adenocarcinoma without laser capture microdissection. Methylation frequencies of all genes in tumor samples were considerably lower than frequencies in microdissected tumour samples (HIC1, 71 versus 89%; p16, 22 versus 78%; GSTP1, 32 versus 100%; N33, 20 versus 33%). The laser capture microdissection is required procedure in methylation studies taking into account multifocality and heterogenity of prostate cancer tissue.
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PMID:[Abberant methylation of p16, HIC1, N33 and GSTP1 genes in tumor epitelium and tumor-associated stromal cells of prostate cancer]. 1738 Aug 94


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